Download Pharm Test 1

Pharm Test 1
Cholinergic agonists – “mimics PNS discharge”
…in general – contract sphincter of iris for near vision (miosis), neg heart stuff, bronchoconstrict, ↑ GI stuff, relax
trigone and sphincter, ↑ secretions, CNS tremor, insomnia, excite stuff; side effects – bad in asthma, hyperthyroidism,
bad heart, peptic ulcers
- Direct Acting – bind and act mus or nico receptors
Esters – 4° amine/polar
Ach – Mx and Nx receptor action; cholase suscept. so short duration
Bethanechol – some Mx; used in GI atony and
Carbachol – some Mx and Nx; used in glaucoma
Methacholine – Mx only
Alkaloids – 3° amine; will X – BBB; acidficat- urine inc clearance cuz add H+
pilocarpine - used in glaucoma
nicotine
muscarine (4°!!!)
atropine to Tx toxicity
- Indirect Acting – bind Achase (in CNS ganglia and postgang parasym and NMJ) or Butyrylcholase (in plasma, liver,
GI, skin and is the MOA of succinylcholine) to ↑ [Ach]; affects a bit more widespread than direct acting ones
reversible
Physostigmine – used in glaucoma; atropine poisoning antidote via comp. antag.
Edrophonium – very polar; reversal agent for NMJ blockers like curare
Neostigmine – myasthenia gravis (along w/ pyridostigmine)
irreversible
“-phates” (incl orgoPO4 fertilizers)
also DFP and parathion
Muscarinic Antagonists – “like E/NE action”
…in general – incl. synthetic 4° amines too; ↑ heart stuff, ↓ GI secretions incl. urinary, bronchodilate, mydriasis (super
dilated eye) and cycloplegia (↓ accommod), ↓ secretions, ↓ CNS @lo dose, but excite and coma @hi dose; side
effects – MAD, HOT, BLIND, RED, DRY (longer w/ atropine due to t1/2)
atropine – nat’lly occur 3° amine; “belladonna look”; ↑ intra-ocular press narrow< glaucoma
benztropine – Tx ParkDz
scopolamine – motion sickness trans-dermal
4° lke ipra- and tio-tropium for COPD et al.
Nicotinic Blocker @ Ganglion
…in general – rarely used cuz not specific so lotsa side effects; block Ach and other nico agonists at nico receptor
hexamethonium/trimethaphan – comp blocker
mecamylamine – non-comp
nicotinic blocker @ NMJ
…in general – used in surgery for paralysis
- depolarizing – cannot be reversed by Achase inh; quick; paralysis from face, small/fast muscles, then goes outward;
adverse effects incl neg heart stuff at smaller dose, ↑ K+, intraocular press, intragastric press (so don’t eat prior to
surgery)
succinylcholine – phase 1 muscles fasiculations from initial discharge, then phase 2 flaccid paralysis
- non-depolarizing – charged; adverse effects – result in histamine release, AG antibiot inh Ach release and will ↑
effects of these non-depol blockers
d-tubocurarine aka curare – comp antag Ach @ nico receptor of NMJ; reverse w/ Achase inh
isoquinolines – above and atracurium and mivacurium
steroids – pancuronium, rocuronium, et al.
Adrenergic Agonists
all have varying degrees of affinity to  (E most) and  (Isopro most) receptors.
 receptor activation – GTP, PL-C, 2nd messenger IP3 or DAG, Ca influx; both act postsynaptically and 1 adds
presynaptic action and also LOTSA of them; vasoconstrict in VSM; 2 in  cells of pancreas
1 – heart, fat, JG renin release, 2 – vascular and airway smooth muscle
 receptor activation – GTP, cAMP, pKA to Ca influx; leads to ↑ contractile and hr, so rhythm problems in these Rx,
relaxation in VSM
-catecholamines – NOT given orally
Isoproterenol – mostly 2 receptor action so vasodilate and ↓ TPR, good in airway dys-fxn Tx
Epinephrine – 2 at low dose for muscle relaxation and ↓ TPR, but high dose will bind 1 receptor as well
and mainly vasoconstrict instead
NorEpinephrine – a1 at low dose, but can act on b as well if high dose; acts at presynaptic 2 receptors to
inhibit own release
-cat @ beta receptor
DA (Dobutamine, a synethetic, acts only on 1 to help CHF) – DA1 receptor in renal vascular bed to ↑ RBF
and hence output; 1 to ↑ force of myocard contraction (+ inotropism); high doses act  receptor and bad arrhythmias
-non-cats – longer t1/2 since no COMT reaction
direct 1 agonist
phenylephrine (incl pseudoephedrine)  vasoconstrict nasal vesels to decongest
imidazolines (oxymetazoline and tetrahydrozoline)  eye drops
methoxamine, metaraminol  hypotension
ephedrine – mixed action
indirect  1 agonist  these 2 below cause mood stimulation, ↑ systemic arterial bp, arrhythmias
amphetamine – incl methylphenidate (Ritalin)
cocaine – blocks NE reuptake
tranylcypromine – MAOI for HTN and depression
albuterol (Ventolin) – selective 2 agonist; act by ↑ cAMP levels; in relaxation eg asthma, bronchitis,
emphysema, premature labor
inhibit storage
reserpine – lyses storage granules
guanethidine – inh Ca-dep release of NE
a2 agonists as smypatholytics  stimulation to cause decrease sympathetic outflow (anti-HTN), ↓ TPR
methyldopa – prodrug, so must be converted first
clonidine – withdrawal, vascular HA, diabetic diarrhea, 2nd line HTN drug
side effects – drowsiness, dry mouth
Adrenergic Antagonists
a1 antagonists – can cause postural hypotension (drops bp too much!)
prazosin and its analogs – selective, competitive for HTN by relaxing vessel walls; adverse – fluid retention
and ↑ cardiovascular event risk
Tamsulosin – selective (1A type!), comp for Benign Prostatic Hypertrophy
both a1 and a2 antagonists – Phenotolamine (nonsel, comp) and Phenoxybenzamine (irrev receptor) –
pheochromocytoma (excess E by adrenal medulla)
beta blockers – can have behave like agonist with low intrinsic activity, can stabilize membranes, screw with endocrine
system; side effects incl fatigue, hypotension, bradycardia, ↑ trigly, ↓ HDL
b1 receptor – heart, renin release; b2 receptor – airways; good for HTN, ischemic heart Dz, CHF, SVT
Propranolol – nonselective so can block airway or VSM (bad in airway Dz or peripheral vascular Dz).
Labetalol, carvedilol – blocks beta AND a1 receptors; Tx HTN and CHF respectatively